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Department of Pharmacology (V.L., G.R., F.S., A.T., V.D.G.C., M.B., E.E.M., F.B.), and Institute of Pharmacological Sciences (G.R.), University of Milan, 20129 Milan, Italy; and Europeptides (R.D.), Argenteuil 95100, France
Address all correspondence and requests for reprints to: Prof. Ferruccio Berti, Department of Pharmacology, Via Vanvitelli 32, 20129 Milan, Italy. E-mail: Ferruccio.Berti{at}unimi.it
We previously reported that induction of selective GH deficiency in the rat exacerbates cardiac dysfunction induced by experimental ischemia and reperfusion performed on the explanted heart. In the same model, short-term treatment with hexarelin, a GH-releasing peptide, reverted this effect, as did GH. To ascertain whether hexarelin had non-GH-mediated protective effects on the heart, we compared hexarelin and GH treatment in hypophysectomized rats. Hexarelin (80 µg/kg sc), given for 7 days, prevented exacerbation of the ischemia-reperfusion damage induced by hypophysectomy. We also demonstrate that hexarelin prevents increases in left ventricular end diastolic pressure, coronary perfusion pressure, reactivity of the coronary vasculature to angiotensin II, and release of creatine kinase in the heart perfusate. Moreover, hexarelin prevents the fall in prostacyclin release and enhances recovery of contractility. Treatment with GH (400 µg/kg sc) produced similar results, whereas administration of EP 51389 (80 µg/kg sc), another GH-releasing peptide that does not bind to the heart, was ineffective. In conclusion, we demonstrate that hexarelin prevents cardiac damage after ischemia-reperfusion, and that its action is not mediated by GH but likely occurs through activation of specific cardiac receptors.
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